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J. Bacteriol. doi:10.1128/JB.00824-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Short-tailed Stx-phages exploit the conserved YaeT protein to disseminate Shiga toxin genes amongst enterobacteria

Darren L. Smith, Chloë E. James, Martin J. Sergeant, Yan Yaxian, Jon R. Saunders, Alan J. McCarthy, and Heather E. Allison*

* To whom correspondence should be addressed. Email: hallison{at}liverpool.ac.uk.


   Abstract

Infection of E. coli by Shiga toxin-encoding bacteriophages (Stx-phages) was the pivotal event in the evolution of the deadly Shiga toxin-encoding E. coli (STEC), of which serotype O157:H7 is the most notorious. The number of different bacterial species and strains reported to produce Shiga toxin now totals more than 500, since the first reported STEC infection outbreak in 1982. Clearly Stx-phages are spreading rapidly, but the underlying mechanism for this dissemination has not been explained. Here we show that an essential and highly conserved gene product, YaeT, which has an essential role in the insertion of proteins in the Gram negative bacterial outer membrane, is the surface molecule recognised by the majority (ca.70%) of Stx-phages via conserved tail spike proteins associated with a short-tailed morphology. The yaeT gene was initially identified through complementation and its role confirmed in phage binding assays with and without anti-YaeT antiserum. Heterologous cloning of E. coli yaeT to enable Stx-phage adsorption to Erwinia carotovora and the phage adsorption patterns of bacterial species possessing natural yaeT variants further supported this conclusion. The use of an essential and highly conserved protein by the majority of Stx-phages is a strategy that has enabled and promoted the rapid spread of shigatoxigenic potential throughout multiple E. coli serogroups and related bacterial species. Infection of commensal bacteria in the mammalian gut has been shown to amplify Shiga toxin production in vivo, and the data from this study provide a platform for the development of a therapeutic strategy to limit this YaeT-mediated infection of the commensal flora.




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